Hydrogen sulfide inhibits nitric oxide production and nuclear factor-κB via heme oxygenase-1 expression in RAW264.7 macrophages stimulated with lipopolysaccharide

Oh, Gi‐Su; Pae, Hyun‐Ock; Lee, Bok-Soo; Kim, Byeong-Nam; Kim, Jong‐Moon; Kim, Hyung‐Ryong; Jeon, Seon Bok; Jeon, Woo Kyu; Chae, Han-Jung; Chung, Hun‐Taeg

doi:10.1016/j.freeradbiomed.2006.03.021

Cited by 402 publications

(320 citation statements)

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“…Conversely, H 2 S inhibits NO generation and expression of inducible NO synthase (iNOS) in LPS-exposed macrophages through a mechanism that also appears to involve up-regulating heme oxygenase-1 (Oh et al 2006). The effect of H 2 S on the response to NO is more complicated.…”

Section: Discussionmentioning

confidence: 99%

Hydrogen Sulfide, a Gaseous Transmitter, Stimulates Proliferation of Interstitial Cells of Cajal via Phosphorylation of AKT Protein Kinase

Huang

Tong

et al. 2010

Tohoku J. Exp. Med.

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Section: Discussionmentioning

confidence: 99%

Hydrogen Sulfide, a Gaseous Transmitter, Stimulates Proliferation of Interstitial Cells of Cajal via Phosphorylation of AKT Protein Kinase

Huang

Tong

et al. 2010

Tohoku J. Exp. Med.

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“…7,8 However, NaHS also impairs aortic vascular smooth muscle cell proliferation by interfering with mitogen-activated protein kinase (MAPK) activation. 9 H 2 S can induce an upregulation of antiinflammatory and cytoprotective genes including heme oxygenase-1 (HMOX1) 10,11 cytochrome c oxidase subunit v, vascular endothelial growth factor (VEGF), insulin-like growth factor (IGF) receptor and several genes associated with the transforming growth factor-b (TGF-b) receptor pathway. 12 Besides, experimental data in animals show that an enhanced production of endogenous H 2 S contributes to the pathophysiology of the organ injury associated with sepsis and shock.…”

mentioning

confidence: 99%

Hydrogen sulfide impairs keratinocyte cell growth and adhesion inhibiting mitogen-activated protein kinase signaling

Gobbi

Ricci

Malinverno

et al. 2009

Laboratory Investigation

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The effects of exogenous hydrogen sulfide (H 2 S) on normal skin-derived immortalized human keratinocytes have been investigated in detail. We show in vitro that exogenous hydrogen sulfide reduces clonal growth, cell proliferation and cell adhesion of human keratinocytes. H 2 S, in fact, decreases the frequency of the putative keratinocyte stem cell subpopulation in culture, consequently affecting clonal growth, and impairs cell proliferation and adhesion of mature cells. As a mechanistic explanation of these effects, we show at the molecular level that (i) H 2 S reduces the Raf/MAPK kinase/ERK signaling pathway; (ii) the reduced adhesion of sulfur-treated cells is associated to the downregulation of the expression of b4, a2 and a6 integrins that are necessary to promote cell adhesion as well as anti-apoptotic and proliferative signaling in normal keratinocytes. One specific interest of the effects of sulfurs on keratinocytes derives from the potential applications of the results, as sulfur is able to penetrate the skin and a sulfur-rich balneotherapy has been known for long to be effective in the treatment of psoriasis. Thus, the relevance of our findings to the pathophysiology of psoriasis was tested in vivo by treating psoriatic lesions with sulfurs at a concentration comparable to that most commonly found in sulfurous natural springs. In agreement with the in vitro observations, the immunohistochemical analysis of patient biopsies showed a specific downregulation of ERK activation levels, the key molecular event in the sulfur-induced effects on keratinocytes.

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“…H 2 S sulfhydrates the p65 subunit of NF-κB at cysteine-38, which promotes its binding to the co-activator ribosomal protein S3 (RPS3) [51]. H 2 S inhibits NO production, iNOS gene expression and NF-κB activation in LPSstimulated macrophages cells via a mechanism involving the action of heme oxygenase-1 (HO-1) and CO [118]. Finally, the pro-apoptotic or anti-apoptotic effects of NO depends on the concentration of NO employed, i.e.…”

Section: The Roles Of H 2 S and No In Apoptosismentioning

confidence: 99%

Hydrogen Sulfide and Endothelial Dysfunction: Relationship with Nitric Oxide

Altaany¹,

Moccia²,

Munaron³

et al. 2014

CMC

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The endothelium is a cellular monolayer that lines the inner surface of blood vessels and plays a central role in the maintenance of cardiovascular homeostasis by controlling platelet aggregation, vascular tone, blood fluidity and fibrinolysis, adhesion and transmigration of inflammatory cells, and angiogenesis. Endothelial dysfunctions are associated with various cardiovascular diseases, including atherosclerosis, hypertension, myocardial infarction, and cardiovascular complications of diabetes. Numerous studies have established the antiinflammatory, anti-apoptotic, and anti-oxidant effects of hydrogen sulfide (H 2 S), the latest member to join the gasotransmitter family along with nitric oxide and carbon monoxide, on vascular endothelium. In addition, H 2 S may prime endothelial cells (ECs) toward angiogenesis and contribute to wound healing, aside to its well-known ability to relax vascular smooth muscle cells (VSMCs), thereby reducing blood pressure. Finally, H 2 S may inhibit VSMC proliferation and platelet aggregation. Consistently, a deficit in H 2 S homeostasis is involved in the pathogenesis of atherosclerosis and of hyperglycaemic endothelial injury. Therefore, the application of H 2 S-releasing drugs or using gene therapy to increase endogenous H 2 S level may help restore endothelial function and antagonize the progression of cardiovascular diseases. The present article reviews recent studies on the role of H 2 S in endothelial homeostasis, under both physiological and pathological conditions, and its putative therapeutic applications. Endothelial structure and functionThe endothelium lines the luminal surface of the entire vascular tree and the cardiac chambers, where it is termed endocardium. As a consequence, the endothelium presents a rather broad extension (300 to 1000 m 2 ) and weight (1.5 kg), achieving sizes comparable to other vital organs of the human body [1,2]. The endothelium can, therefore, be regarded as a real "organ spread across the organism" [3] and, as such, not only it is important for the regulation of local tissue functions, but also for maintaining the whole organism homeostasis [4]. Vascular endothelial cells (ECs) possess a polarized architecture: their luminal membrane is directly exposed to hematic constituents and circulating cells, while the basolateral surface is separated from surrounding tissues by a glycoprotein basement membrane -the sub-endothelial basement -which is formed by fibronectin, laminin, and collagen and is secreted by ECs themselves [2].Heterogeneity is, however, the hallmark of endothelium. ECs differ in morphology, function, and gene expression profile, so that even neighbouring cells from the same organ and blood vessel type exhibit distinct features [4]. For instance, vascular ECs may vary in size, shape, thickness and position of the nucleus. Albeit oriented along direction of blood flow, to attenuate the impact of shear stress forces on the vascular wall, microvascular ECs are rather thin (0.1 µm) and spindle-like, whilst their macrovascul...

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Hydrogen sulfide inhibits nitric oxide production and nuclear factor-κB via heme oxygenase-1 expression in RAW264.7 macrophages stimulated with lipopolysaccharide

Cited by 402 publications

References 50 publications

Hydrogen Sulfide, a Gaseous Transmitter, Stimulates Proliferation of Interstitial Cells of Cajal via Phosphorylation of AKT Protein Kinase

Hydrogen Sulfide, a Gaseous Transmitter, Stimulates Proliferation of Interstitial Cells of Cajal via Phosphorylation of AKT Protein Kinase

Hydrogen sulfide impairs keratinocyte cell growth and adhesion inhibiting mitogen-activated protein kinase signaling

Hydrogen Sulfide and Endothelial Dysfunction: Relationship with Nitric Oxide

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